Tebentafusp (IMCgp100) is a bispecific fusion protein to target gp100 peptide-HLA-A*02:01 (a melanoma-associated antigen). Tebentafusp guides T cells to kill gp100-expressing tumor cells via a high affinity T-cell receptor (TCR) binding domain and an anti-CD3 T-cell engaging domain. Tebentafusp leads to inflammatory cytokines and cytolytic proteins production, resulting in the direct lysis of tumour cells[2].In Vitro:Tebentafusp is an ImmTAC recognizing a peptide derived from the melanoma-specific protein, gp100, presented by HLA-A*0201.
Tebentafusp (31 pM, 82 pM, and 131 pM; 16 h) stimulates cytotoxic degranulation activity of PBMC against Mel526 cells rather than gp100-negative A375 cells.
Tebentafusp (100 pM; 0-50 h) mediates CD8+ T cell killing despite the presence of regulatory T cells via monitoring caspase 3/7 activation during 40-48 hr.
Tebentafusp (100 pM; 0-80 h) triggers cytolysis of melanoma cells by CD4+ T cell subpopulations.
Tebentafusp (1, 12, 31, 82, and 131 pM; 24 h or 96 h) increases granzyme B amount, and induces broad cytokine and chemokine release including in both CD4+ and CD8+ cells.
In Vivo:Tebentafusp (10 μg/kg; i.v.) inhibits tumor growth in mouse melanoma model.